**1. Introduction**

Autoimmunity occurs when a component of a certain tissue of the human body becomes immunogenic with consequent production of autoantibodies against it. For induction of autoimmunity three conditions are required.

a.Self-antigen.

b.An inflammatory environment.

c.A genetic predisposition.

For the production of a self-antigen, two mechanisms are implicated. A part of an inflammatory agent, a virus, for instance, may have similarities with a component of human tissue and in this way it becomes immunogenic; this mechanism is called molecular mimicry – a mechanism quite commonly encountered in nature. Another mechanism is epitope spreading when fragments of damaged tissue during the inflammatory process become immunogenic. Stimuli that may induce an inflammation are multiple: microbes, viruses, chemicals, stress, etc. As all human beings are exposed to various agents very frequently, it is quite difficult to identify the initial moment autoimmunity occurs and the responsible factor [1].

## **2. Lupus erythematosus**

Lupus is the prototype of autoimmune diseases with B-cell hyperactivity resulting in the production of anti-DNA autoantibodies and manifests with abnormalities of internal organs. Renal insufficiency, hemolytic anemia, arterial and venous thromboses are common in SLE. Skin eruptions may also be observed in patients with SLE. Females are more frequently affected with the disease female: male ratio 6-10:1. Prevalence of SLE is relatively low 1 in 2000, in general population. Despite this fact, SLE remains an important health care problem and is associated with a significant financial burden to the community because of the young age of the individuals suffering from the disease. A study of survival from 2000 to 2002 has shown that almost 4% of all patients hospitalized in New York AND Pennsylvania with lupus die [2, 3].

Lupus is a disease with a strong genetic component as it runs in families [4].
